An estimated 60% to 84% of patients with cancer develop bone
metastasis. Of these 70% experience pain syndrome which is difficult to
manage, of which 50% die without adequate pain relief with a poor
quality of life. It is therefore necessary to have accessible and
effective medications for the management of this condition. One of the
most common pain syndromes in patients with advanced cancer is bone
metastasis. This is difficult to manage and control in clinical
practice. Currently, scientific advances in cancer detection and
treatment have prolonged life expectancy in patients. Unlike the case
with the phenomenon of bone pain in cancer, where current treatment
strategies are not significantly effective. Most palliative treatment of
bone pain are based on clinical studies on pain management in patients
or in experimental models is not well designed this could explain why
the drugs used are partially effective. Today, one of the main obstacles
in developing new, safe treatments to control bone pain is the absence
of basic science knowledge in the physiology of bone pain.
Epidemiology
The
pain in cancer patients is usually multifactorial, may arise from the
process itself, treatment side effects or both. For these reasons the
approach and management of this symptom should be multidisciplinary.
Pain syndrome occurs either by local proliferation or tumor invasion of a
metastatic tumor from a distance. With metastatic bone pain often
reflects the presence of a tumor in breast, thyroid, prostate, kidney,
lung or adrenal.
Physiology of bone pain
Bone pain is
associated with tissue destruction by osteoclast cells. Normally,
osteoclastic bone resorption are in balance with bone formation mediated
by osteoblasts. In neoplastic osteolytic activity is increased and
there are substances such as cytokines, local growth factors, peptides
similar to parathyroid hormone and prostaglandins. Autacoids are also
released other owners as potassium ions, bradykinin and osteoclast
activating factors. These tissue substances play an important role in
sensitizing the neural tissue against chemical and thermal stimuli,
lower thresholds for discharge of the neuronal membrane, produce
exaggerated responses to stimuli above the threshold and result in
discharges of tonic impulses normally silent nociceptors. This
phenomenon is called peripheral sensitization and primary hyperalgesia
and is understood as events occurring within the ranks of the injured
tissue and stimulate peripheral nociceptors (C fibers and A delta
fibers) translating pain. In bone tissue of the sensory receptors are
located primarily in the periosteum, whereas the bone marrow and bone
cortex are insensitive. This phenomenon of peripheral sensitization
results in abnormal sensitivity to pressure surrounding skin (allodynia
and hyperalgesia), pain in muscles, tendons, joints and deep tissues in
contact with bone. This is limited to ensure that the peripheral ends
have a greater capacity for alarm response to injury.
The constant
presence of harmful process, stimulating nociceptive receptors gives
the introduction of a subacute pain that tends to be chronic with the
growth of bone metastases. These stimuli lead to another prevalent
phenomenon called central sensitization important which includes
abnormal amplification of incoming sensory signals to the central
nervous system, particularly the spinal cord. The phenomenon occurs
because of the persistent input stimulus through the fibers C. This
spinal cord triggers a temporary increase in the power of silent
synaptic terminals. In this process plays an important role of glutamate
receptor N-methyl-D-aspartate (NMDA). The resulting amplification of
the signal generated in the postsynaptic neuron sends a message to the
brain which is interpreted as pain. In short central sensitization
amplifies the sensory effects of both peripheral nociceptive inputs (C
fibers of pain) and non-nociceptive fibers (A of touch).
In
practice the two phenomena come together in the genesis of metastatic
bone pain and peripheral sensitization occurs acutely metastatic lesions
to appear nociceptors and translate the information conveyed through
the afferent myelinated A-delta or unmyelinated C fibers to the spinal
cord where the information is modulated by various systems. With the set
up process subacute begins the process of central sensitization which
sensory synapses begin to activate silent. And there is a state of
increased central perception. By becoming chronic pain phenomenon
becomes even more complex because all that is in contact with the area
of injury becomes a powerful generator of pain. The touch, muscle
movement or joint pain result, manifesting the phenomena of allodynia
and hyperalgesia much more marked.
With progression and growth of
metastatic disease can appear phenomena of compression of peripheral
nerves, nerve roots or spinal cord. Then the pain can refer to other
dermatomes, further complicating the initial picture painful. This
condition becomes a debilitating factor for the patient and to be
inadequately controlled could trigger the phenomenon of total pain
detailed below.
I M Currently doing my doctorate and felt immense need to help the people about the Bone Cancer